Objective. To identify pathogenetic factors of the development of infection-dependent chronic inflammation in the bronchi and secondary bronchiectasis in patients with chronic obstructive pulmonary disease.

Materials and methods. 135 patients with chronic obstructive pulmonary disease (COPD) were observed. The nature of sputum secreted, the intensity of bacterial colonization of the bronchi, and the results of bronchoscopy were important in detecting chronic infection-dependent inflammation in the bronchi at different stages of COPD progression. Bronchography was performed in 52 patients and computed tomography was performed in 83 patients to detect secondary bronchiectasis and its prevalence in the bronchi, depending on the stage of COPD development.

Results. At the first stage of COPD, 75.0% patients had no infection-dependent inflammation in the bronchi, catarrhal toxic endobronchitis was detected in 25.0%. In the second stage of COPD, catarrhal endobronchitis was 18.7%, atrophic — 68.7%, hypertrophic endobronchitis — 12.5%. At the third and fourth stages, purulent endobronchitis was detected in most patients (37.0% and 77.8%, respectively). At the second stage of COPD secondary bronchiectasis were detected in
12.5% of patients, at the third stage it was observed in all patients in the lower lobes, at the fourth stage in 82.4% of patients, secondary bronchiectasis was noted in both the lower and upper lobes.

The first factor in the mechanism of development of infection-dependent chronic inflammation in the bronchi and secondary bronchiectasis is the increasing fibrous transformation of lung tissue and obliteration of small bronchi mainly in the lower lobes under the influence of exogenous stimulus.

The second factor is a persistent embarrassment of ventilation.

These two factors are formed for many years, and other factors appear when increasing fibrosis leads to the depletion of breathing reserves.

The third factor is a disfunction of the processes of self-cleaning of the bronchi due to poor ventilation.

Due to the ineffectiveness of the processes of self-cleaning of the bronchi, a fourth pathogenetic factor arises – chest congestion, which serves as a breeding ground for bacteria.

The fifth factor is bacterial colonization of the bronchi by opportunistic microflora.

The sixth factor is the development of infectious-dependent chronic bronchitis.

Chronic inflammation in the bronchi leads to the appearance of the seventh pathogenetic factor — the development of connective tissue in the mucous membranes and deep layers of the bronchial walls with its scsrry transformation. The fibrous tissue in the bronchi undergoes stretching, and gradually bronchiectasisform on the spots of scars (the eighth factor).

After the occurrence of secondary bronchiectasis constant contamination of the bronchi of neighboring segments leads to the development of chronic infection-dependent endobronchitis and recurrent secondary pneumonia there with gradual replacement of the alveoli and bronchioles with scar tissue (the first factor), which leads to embarrassment of ventilation (the second factor). Thus, the first two pathogenetic triggers are formed and the following 6 factors are successively added, which are already active in the bronchi of the upper lobes of the lungs.

Conclusion. The sequence of formation of pathogenetic factors for the development of chronic nonspecific infection-dependent inflammation and secondary bronchiectasis in the bronchi in COPD has been established. The triggers factors are slowly increasing pneumofibrosis and impaired ventilation. Featureless infectious-dependent chronic inflammation in the bronchi occurs in the 2nd stage of COPD development. At this stage it is inversive if the effect of exogenous stimuli stops. At stages 3 and 4 of COPD development, pronounced pneumofibrosis and emphysema are accompanied by significant embarrasments of ventilation and self-cleaning processes of the bronchi, and therefore the progression of infection-dependent chronic inflammation and the formation of bronchiectasis continues even after the cessation of exposure to exogenous stimuli. Prevention of recrudescences of the infectious-dependent chronic inflammatory process in the bronchi at stages 3 and 4 of COPD development is achieved by using methods of therapeutic bronchoscopy, which, eliminating the impact of the 4 pathogenetic factor, can eliminate inflammation in the bronchi and stop the progression of COPD.